Nephrology - Dr Abo-ElAsrar - By El Azhar Medical Students 2012

8/13/2019 Nephrology - Dr Abo-ElAsrar - By El Azhar Medical Students 2012

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( BETA EDITION)

With

Prof. Dr Mohammed Abo El-Asrar

Edited By

El-Azhar Medical students 2012


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Nepgrology Dr. Abo-Asrar

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Nephrology INDEXTotal pages = 47

Total time = about 9.5 hours

number Pa- lecture 11 4 - 5

Introduction ( page 4 ) inheritance 6 ( Autosomal inheritance 6 )

2- lecture 12 5 - 1

cont. Introduction ( page 5 ) 3- lecture 13 12

Nephrotic $ ( page 12 )

4- lecture 14 19 -

cont. minimal change ( page 19 )congenital nephrotic ( page 21 )

5- lecture 15 25 -

cont. post str. GN ( page 25 )introduction to RF ( page 26 ) .. 6- lecture 16 32 -

cont. introdiction to RF ( page 32 )

chronic RF ( page 34 )

7- lecture 17 39 -

acute RF ( page 39 )

Urinary Hues ( page 44 )Hematuria ( page 45 )


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Nepgrology Dr. Abo-Asrar

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Nephrology Prof. Dr. Abo El-Asrar

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11....1:27

NEPHROLOGY 4

- nephrotic syndrome ( $ )2- nephritic syndrome ( $ )3- renal failure4- hematuria glomeruliBoumman's capsule + glomeruli capillary tuft affernentefferent ff.ff. pressureglomerulusB. capsule plasma proteinplasma

- filterate3 layers():- basement membrane of kidney ( ) 2- endothelium of capillaries ( (3- epithelium of B. capsule ( )

capillariesendotheliumfilteratebasement memfenastraepitheliumB. capsule

layers- ( :the basement membrane ( BM endotheliumepithelium- BM

BMcalled anatomical fenestra sialo protein (ionaizable)ve charge magnetic fieldanatomical fenastramagneticphysiological fenastra

--p. proteinurine

..glomerulus sheding of mucoprotein that cover cells of tubules

urine< 30 mg / 24 hrs


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glomerulus :-anatomical

high molecular weight proteinglobulinhaptoglobinephysiological- .As crystalloids as Na, K, etc

anatomicalphysiological-So, should pass through the magnetic field

A - So, if +ve charged -Hbintravascular hemolysisHb

And leading to acute tubular necrosis

B but if ve : LMW protein(ve)ve charge-

As albumin , transferring , IgG , tuftsin , lipoprotein lipase ( which destruct cholesterol ) , protein C

protein S & antithrombin iii

sialo proteinLMW protein(HMW protein)selective proteinuria sialproteinselective BMLMW+HMW

non selective proteinuria12 2 afferentefferentAnd aff. : eff. = 7:1 WHY ??To increase the pressure inside the glomerular capillaries

(pressure( glomerular filterateplasma protein sialoproteinselective proteinuria

- in the most common type of nephrotic $ minimal change nephrotic

2- also, in congenital nephrotic $

2elective proteinuria BMnon selective proteinuria


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-proteinuria urine...urine :Protein in urine >= 150 mg/24 hrs urine 4

30150..30-Called microproteinuria may be treatable or complicated by macroproteinuria ( 150 mg )

- Grades of proteinuria - if protein in urine 150-500 mg/24 hrs urine mild proteinuria

2- if > 500 & < 2000 moderate as 1 gm /24 hrs

3- if >= 2000 mg ( 2 gm ) heavy or massive

- ( silaproteindestruction of BMnephrons - Heavy proteinuria hypoprotenmia

what is the effects ??

plasma protein in urine plasma protein hypoproteinemiavenous sidearterial sidecapillaries

capillaryo2nutrientswaste products water....-

- interstitial spaceinterstitial space ()osmotic pressure25 mmHgplasma prhydrostatic pressure

- in arterial side 32 mmHg- venous side 12 mmHg

1 mmHg1 liter of water arterial end=25 X 1=25*=32 =32-25=7interstitial space(nutrients(O27 venous side=125=25*=12(25-12=13)


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aste productslood(3 713/7=1.5..interstatiumarterial end1.5venous end( )

interstitial space odema:hypoproteinemia-

Due to :A - osmotic pressure say 15 ( not 25 as normal ) arterial side17(32-15=17)interstitial space() venous side3(15-12=3) interstatium14()massive odemageneralized osmotic pressure

odema-ADH : interstatium))14venous sidearterial side atriaatriavolume receptors

hypotha ADHkidneyto collecting tubulesurine reabsorption ..osmoticpres urineADH osmotic pressure.

renine aldosterone VRCOPVR COP renal Bl. Flow juxtaglomerular apparatusafferentcolumnar cellsif RBF secrete renine hormone convert angiotensongen to angiotensen I then to ii to supra

that secrete aldosterone to distal tubules reabsorption of Na then Na take water tointravascular osmotic pressure odema

-hyperlipedemia or hypercholestremia :


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osmotic pressureliversynthesis of albumin as a compensation kidneyurine

liver cellsmarked hyperactivityover compensationalbumin..cholesterollipoproteins

intake- liver(liver)NB. liver

need lipoprotein lipasewhich is one of LMW protein that lost in urine (so, hyperlipedemia or hypercholestremia-ephrotic

clinical $ that characterized by heavy proteinuria , hypoprotenmia , massive generalized odema with

without hypercholetremeia )heavy proteinuria = >= 2 gm/24 hrs )

childadultproteinuriagrades- nephrotic

osmotic pressurealdosterone-osmotic pressureosmolarity -

)urea(Na extravascularintravascular body fluidsNB. All called extracellular fliud

depends on plasma protein that only intravascular

odemaas a drainage systemlymphatic system-

odemaarmlymphatic.. - :: :

- odema of BM fenastra 3proliferation of endothelium proliferation of epithelium of B. capsule2


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glomerular filtration-- so , oliguria

--urine24

- if < 400 ml / m2 surface area/24 hrs = oliguriam2 surface area =

-urface area chart3columns surface areaheight surface area()7 + ( 4 Wt ) / 90 + Wt ( not accurate )

400surface area200.....

oliguria- Anuria < 180 ml / mm2 SA / day

- absolute anuria NO urination ..hypervolemia

hypertension intravascular pressure

osmotic pressurehydrostatic..:arterial side say 36 * - venous side say 15 ..at the arterial side 36-25 = 11 liter water .at the venous side 25-15 = 10 liter water 1(14)mild odema

that appears only in dependant areas knee & elbow positiondependant areas as : - puffines of the eyelids


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.. dorsum of the hands & footsodema intravascular pressurecapillaries

so, may episcapillaries pressure( bleeding(..)Hematuria plasma protein

as here there is hematuria that contain not only RBCs but also plasmamild proteinuria

non-selectiveboth H&LMW protein selectivenon selective--nephritic $

- that defined as clinical $ characterized by oliguria , hypertension , hematuria , mild odema & mild

proteinuria

((-(nephritic)surface area1 m2200

1that indicate severe hypertension

urine200 ml/day(oliguria.. )criterianephritic200,000..2nephrons capllairesBM :of nephrons) %10)

hematuria become frank + protein heavy proteinuria ( > 2 gm / day )

urine output 350 ml ( still oliguric )

Bl. Pressure become 160/120 but still hypertensiveosmotic pressure so, massive odema ( due to heave proteinuria )

-:- still oliguria

2- still hypertension3- hematuria

4- odema

5- preoteinuria

- called nephritic nephrotic $ 45 - causes & Pathogenesis :

-nephroticnephritic


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WHAT IS THE ETIOLOGY ?

- congenital congenital nephrotic $ sialoprotein

- so, heavy selective proteinuria hypoproteinemia massive generalized odema

& if healthy liver hypercholetremia but if diseased liver no hypercholestremia2- immunemediated A- direct antigen antibody reaction part of the kidney is antigenic reaction

sialoproteinselective heavy proteinuriaAbs-one of nephrotic called minimal change nephrotic $

B- destruction of the basement membrane ( BM )

non selective proteinuria and other manifestations of nephrotic

- as in membranous glomerulonephritis ( GN ) or rapidly progressive GN

C- also, antigen antibody reaction proliferation in the kidney - so, proliferation of endothelium or epithelium of B. capsule or odema of BM

Nephritic $ or may complicated by nephrotic

D- Immune complexes complement..antigen-antibody c1-c9kidneyand cause nephritc,nephrotic or both-

-investigations-3.. classic pathwayso, consumed in any complement aggregations

So, 1- if C3 means immune complex mediated pathology

2- if normal C3normalcongenital nephrotic $-

minimal change nephroticC3normalpost.streptococcal GNC3immune complexes

complementimmuno fluoresceinbiopsyslide fluorescenceslidelight microscopefluoresceincomplementwashingslidefluoresceinimmune complex

so, if C3 so, +ve immuno fluorescein test

- so, in congenital -ve * in minimal change -ve * post. Strept. +ve

-Ml


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linear on glomeruli or lumbi deposition - if linear depositions on tha whole BM

-kidneyantigenic2- if lumbi depositions

immune complexkidney - (linear)end stage RF inear 100 32

Nephrotic syndromeDefinition

Clinical condition that characterized by 1- heavy protenuria

2- hypoproteinemia

3- massive genarlized odema

4- +/- hypercholetremia

Etiology : 1ry & 2ry

-1rypathology(: )- congenital Nephrotic $

2- minimal change nephrotic $

3- membranous GN.

4- focal GN.

5- membrano-proliferative GN.

6- rapidliy progressive GN.

ystemic diseases- collagen diseases as SLE ( multi systems affection )

-lupuskidneyaffected2- Endocrine diabetic nephropathy 5 3- allergic vasculitis blood

- as Henoch shoneline purpura


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4- sickle cell anemia immune complex formation

5- lymphoma 6- shistsoma mansoni & malaria

7- drugs as gold , penicllin etc-

- congenital & minimal change pure nephrotic only & the rest either nephritic , nephrotic or bot- ascities , scrotal odema , puffiness of the eyelid

generalized odema urine analysisalbumin+ 4(means about 2.5 gm / 24 hrs)total protein 3 gm - serum albumin 2 gm ( hypoproteinemia )

-ephroticQ : enumerate causes & discuss how to diagnose one of them ??

dorsum of hand & footodemapuffinessurine analysis RBCs in urine

urine output < 400 ml / m2 + headache

ephritic-- congenital 2- minimal change -

NB . most common cause of nephrotic minimal change = 70 % of all pediatric nephrotic.. minimal change nephroticMinimal change nephrotic- Cause autoimmune

antibodies against sialoprotein selective heavy proteinuria

improves by measles infection due to suppression of T-cells all autoimmune process measlesinfectionTB- male > female 2:1 2- most common cause of nephrotic $

3- age of onset

2-7 years -angeare are- Clinically (!!!.. )():

1 - ONLY massive generalized odema


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eyelid.... puffiness of eyelid then extremites ( dorsum of hand & foot )

then genetalia ( scrotal in male labial in female ) + L.L odema

abdominal & chest wall + ascites , pleural effusion & pericardial effusion

causes of this odema - osmotic pressure due to plasma protein

2- ADH odema

3- aldosterone Na & water retention more & more odema

2- important ve data :- No oliguria No hematuria No hypertension nephritic

- nephroticmanifestationsgeneralized odema-odemarenalby exclusion of other causes of odema:

- cardiac L.L then ascites then allover the body 2- liver disease ascites then L.L then allover the body

3- nutritional odema with loss of Wt

no history of cardiac or liver diseases

-Either nephrotic or nephritic-nephrotic

-nephrotic : ..NBhypertension may occurs in 10-20% of minimal change N

complications- may present with complication of nephrotic

-2 complicationsA - incidence of infections - odema precipitating factor for infection

"".. organism..

2- loss of 2 important immuno components in urine


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- loss of IgG & tuftsin ( opsonin ) that help in phagocytosis of capsulated organisms

3- use of immuno suppressive drugs in the ttt as cortisone

B - risk of thrombosis 3 - blood viscosity

-..thrombosis- coagulation factors

liver-- coagulation factors

-antithrombin iiiactive factor iiiafibrinogenConvert fibrinogen to fibrin

- antithrombin III lost in urined- loss of protein C & S in urine inactivationcoagulation factors

- WHY blood viscosity ??1- odema interstitum

2- in ttt diuretics used shift water from intravascular to urine

3- cholesterol viscosity

4- polycyathemia due to using os steroids for long term & polycyathemia is onethe most importrant side effect of steroid

- laboratory diagnosis ( investigations ) :- dema

heavy proteinuria-- urine analysis 24 For measurement of total amount of proteins + type of proteins in urine by elsectrophoresis of urine

- protein > 2 gm / 24 hrs ( heavy proteinuria )

protein electrophoresis low molecular Wt protein so, selective ( albumin , trasnsferrin , & IgG ) (

lobulin , no etc all HMW protein (

2- for hypoproteinemia total protein & serum albumin

normal serum level protein = 6-8 gm %

normal abumin = 4.5 5 gm % ( here < 2.5 gm / dl ) WHY ??

- loss of protein in urine


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- gut wall odema gut secretions which is mucous which is protein in nature

-stool- catabolism of protein WHY ??

odematousBMR consumption3- serum cholesterol > 300 mg / dl ( normal level = 150-250 mg % ) WHY ??

- synthesis by the liver

- metabolism due to lipoprotein lipase enz.

4- C3 Normal ( not immune complex )

5- renal functions normal

6- U/S for detection of ascites chest X ray for detection of pleural effusion

7- renal biopsy ( not a routein investigation )

-steroidlight microscope every thing is normal

fluorescein -ve

EM fusion of foot processes-epithelium of B. capsuleBMfoot processfusion sialproteinAbsadhesion minimal change nephrotic $normal..

EMfusion of foot process- TTT : nephrologyttt:

complete rest in bed + 3 D- complete bed rest BMRcatabolism RBFglomerular capillaries pressureerect position()flat position()

- so, flat proteinuria so, loss of protein2- Diet :

Protein fat CHO + minerals + vitamins + water-

- CHO


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- fat due to increased cholesterol ( already increased in this patient )

- protein

pure protein .. ..().. ....fat ....choles. !!!..rickets..vit Dvit D

.. )( 3..100 gm300 gm .. .. )(......!!!.. .. d- minerals salts

-aldosteroneodema- vitamins & water

3- diuretics odema-

lasix loop ( ) K+ loss so, give K +

aldactone weak

blockaldosterone asixldactone(

osmotic diuretics as mannitol IV

..effectlasixsalt free albumin :

osmotic pressure


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bl. Volumeinterstitial space.... )200)albumin kidney..hypervolemiaongestive HF urine..LASIX

compensationliverodema..cholesterol & coagulation factors

.. tepiuretics- diuretics..autoimmune odema(26..20) immunosuppressive drugsKg..ighdose..odema ascitesrenal vessels..renal perfusion..

respimmunosuppressive drugs

immunosuppressive..exclusion to serious infections-urine cultureTB

globulinLMW proteinIgG HMWtglobulin:....diuretics..

4- Drugs immunosuppressive drugs

- cortisone ( prednisone ) 2 mg / kg / day ( max 60 mg / m2 / day ) coagulation(test of proteinuria) albumin free.. () albumin..cortisone

suprarenal shut70%

- monthlbumin(rinerenal biopsy..renal biopsy inimal change..cortisone.. ((

..requent relapser(ocal glomerulosclerosis--ortisone.. cytotoxic drugcortisoneside effects..cortsisone


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6(222)..6 ingle dose cortisone in the early morning every other day ) cytotoxic drug(as cyclophosphamide endoxan)63.. ..3-embrano - proliferative GNincidence of thrombosis .cytotoxic(3) anticoagulant

-embranous & its prognosis :

10 % renal failure

90 % death from complications 43 :D.D. of minimal changenephrotic syndrome in 1styear if life

post streptococcal GN

D.D. of minimal change NS- congenital nephrotic $ autosomal recessive gene() (age of onsetsialoprotein since birth)generalized odema

neonatal peri..inimal change-7 years selective proteinuria..congenital(has no ttt (bad prognosis2- Focal glomerulosclerosis : minimal changepresentationcortisone ..frequent relapsing()3- membranous glomerulonephritis

age of onset not common in pediatrics 0 on-selective(BM) ..prognosis(10% & 90%)4- membrano-proliferative GN : :immune complex..immune complex

C3 + +ve immunoflourscentstydy + EM finding

-BMproliferation of endothelium of capillary tuft & epithelium of B. capsule ..nephriticnephritic nephrotic


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( hypertension , oliguria , hematuria )

- bad prognosis age of onset mainly > 10 years ( )5- 2ry to systemic diseases : other criteria of systemic disease..

cortisone( heavy proteinuria , selective ..)+- diuretics+cortisoneurine.. 2/3(64)..6( )

6cortisone cytotoxic(focal G.sclerosis

3 presented with puffy eyelid & generalized odema , protein in urine 3 gm / 24 hrs

, serum albumin 1.5 gh / dl serum choletreol 400 mg / dl

(4criterianephrotic( ))- enumerate causes & how to diagnose one of them ?? (congential nephrotic..3(..

-15A causes of nephrotic $ in 1styear of life :

1- congenital nephrotic $ ( common )

2- minimal change NS not common ( 2-7 years )

3- membranous GN of idiopathic cause

4- focal g. sclerosis

1- 2ry to infection

- congenital toxoplasmosis

-2ry to infection- syphilis membranous GN 2ry type

-..idiopathic2- 2ry to teratogens :


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lead poisoning arsenic poisoning

-kidney3- 2ry to genetic disease as :

- Nail-Patella $ charectrized by nephrotic + nail atrophy + absent patella

gene factor..1rykidney2ry4- Nephroblastoma ( embryogenic tumor )

5- Hemolytic uremic $ bleeding disordersE-Coliverotoxin(GIT)coagulation+ immune complexesdepositionkidneynephritic+hemolysis in....

B Discuss diagnosis of one of them :

congenital nephrotic $(): congenital nephrotic1- Etiology :

autosomal recessive gene abscent of sialoprotein

2- C/P :- massive generalized odema : pericardial effusionpleural effusionascitesgenetaliaUL & LLpuffiness complicationsnephriticodema ..infection mmunosuppressive

( odema loss of IgG & tuftsin ) .. ..thrombosis teroids (ongenital3- Investigations :

- urine analysis : heavy proteinuria > 3 gm / 24 hrs

2- total serum protein & serum albumin

- choletrerol

3- normal renal function

4- renal biopsy ( diagnostic )

4- TTT : estdiet.. , special milk formulaprotein CHO , low fat , low salt


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diureticscurative tttENAL TRANSPLANTATIONPost streptococcal GNlinicalEtiology & pathogenesis

streptococcal strain ( 12 pharyngitis ) ( 49 skin infection ) 2 strainsAbscomplementimmune complexes glomerulidepositionfilter..irritationproliferationof endothelium & epithelium of B. ca(irritation)also,

juxta glomerular appartus, mesyngemal Diffuse proliferatve GNimmune complexssubendotheliumbetween endothelium & BM not in kidneyantigenic partEMlumbi deposition

odema of BMfenestraGFRoliguria or even anuria then hypervolemia hypertension hysdrostatic pressure mild odema

then some rupture of some capillaries hematuria

-nephritic...C / P

- oliguria & hematuria :

-< 400 ml..(RBCs)frank or smoky2- hypertension :

-headachehypertension- due to GFR - also due to proliferation of juxtaglomerular appartus

renine aldosterone salt & water retention volume of the blood hypertension

immune complexes deposition on endothelium of peripheral vessles irritation & proliferation lu

peripheral resistance hypertension ( called peripheral vasculitis )

3- mild odema : ..mild odema odema of dorsum of the hand & foot ..hydrostatic pressure(hypertension)odemageneralized-

- if complicated with nephrotic


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2- may associated with HF.

3- acute RF without restriction of fliud

- complications :

- hypertension ( congestive HF )

- toxic myocarditis immune complexes - volume overload

- brain odema ICT headache not relived by usual analgesic .. onelived by morhine.

- projectile vomiting not precided by nausea

- convulsion may occur

- Investigations :

- Nephritic or not ?? ( glomerular bleeding or not ?? ) so, do urine analysisa- volume < 400 ml 24 b- specific gravity

-..specific gravity..c- proteinuria mild

d- RBCs casts ( diagnostic ) nephiritis....glomerular hematuria..hematuria BCs

bilharziasis separated RBcs

UTI separated RBcs

stone separated RBcs

tumor separated RBcs

- .... RBCstubule()mucoproteintubule..

2-RBCsbiconcave..2- poststreptococcal or not ?? markersin winter antistreptolysin O titre ( ASOT) due to throat infections


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in summer antihyalouridinase due to skin infections

immune complexes in blood

C3 level

3- Renal biopsy :

LM proliferation ( as it is diffuse proliferative GN )immunoflourscen + ve

EM subendothelial depositions ( lumpi form )

NB complications or not ??clinically ( ) as hypertensive encephalitis or not ( clinically )4- Reanl failure or not ?? do renal function tests

- ttt : streptococci- eradication of streptococcal infection give penicillin for 10 days ( )2- Diet ( )- CHO b- fat RF..ureasuppression to lipoprotein lipase enz.o, cause

hypercholestremia

- protein as urea from protein liver impairmentproteinrenal impairment..d- Na e- K+

f- water so, fluid restriction fluid chart()..:volume of urine / 24 hrs ( ) + 400 ml / m2 ( for extrarenal water loss through

espiration , sweat etc ( ()3- ttt of hypertension ( antihypertensive drugs ) ..4- for hyperkalemia ) K- citrate..

- normal serum K 3.5-5 mEq / L


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7dialysisarrhythemia of heart.. so the toxic level is very very narrow

-- glucose + insulin

-()so, give glucose + insulin

2- bronchodilators : smooth ms of bronchusstimulationB2bronchodilatorshypokalemiasmooth ms of bronchusso, give B2 agonist by inhalation

3- Ca gluconate

-Ca gluconate:brasyarrythemia ( cardioprotective against tachyarryrhemia of K + )

give K-gluconate wcich is fat slouble to liver excreted in bile

4- ion exchange resin :

electrolyte disturbanceion exchange resin-5- peritonial dialysis & its indications are :

persistent hyperkalemia

hypervolemia , urea , creatinine 54:

DD of poststreptococcal GN

introduction to renal failure BM transplant & renal transplant ((RF

- DD of poststreptococcal GN

.poststreptococcal GNtypical nephriticoliguria , hypertension , hematuria , mild odema nephritic $ or acute GN microscopic or macroscopicpoststreptococcal or acute GNhematuriamild odemamild odemaas cardiac or hepatic or nutritional hypertension

- .. - other causes of acute GN :

A - alport $ = heridiatry nephritis

gene factor mainly autusomal dominant


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autosomal recessive or X linkedage of onset 1st6 months or max. 1st12 months

- - nephritic $

2- other manifestations as :

SNHL .. Keratoconus

-.. (transplantation)kidneyB - IgA nephropathy IgAmucosa

infection(viral)IgAmucosa(1stprotective mechanism)serumIgAserum..kidney

(immune complexes.. )depositionodema of BM.. o, all manifestations of neohritic but severe hematuriaproliferationinfection nephritiso, recurrent nephritis ..

..IgA with any infection(hematuria)-

IgA in serum , normal C3 ( also in alport C3 is normal )

biopsy deposites IgA kidney transplant..kidneykidney IgA depositesvoid infections

C - hemolytic uremic $ D - rapidly progressive GN

Renal failureINTRODUCTION

organ failure-so, we must 1stly know functions of the kidney 3

A Endocrinal functions :- erythropiotein

RBCsRBCsanemiastem cells of BMRF..-


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2- thrombopiotein receptorsstem cellsmegakaryocytesmother cells of platlets RFthrmbocytopenia3- as kidney activate vit D so, if failure Rickets ( if still growing bone )

vit D..vit D3ultra violetrays

convert cholestreol to vit D3 ( cholecalcifirol ) wcich is non-functioning vit. hydroxylationsfunctioning vitat C25 give 25 hydroxy cholecalcifirol

hydroxylation at C1 ( parathyroid hormone dependant )

kidneyreceptorsparathrmoneactive form(1-25dihydroxycholecalcifirol) 11-hydroxy(. 1-25 dihydroxy alpha)liver

(.vit D1-25 dihydroxy(4- kidney secrets renine from juxtaglomerular appartus ( )

from columnar cells at the end of afferent arterioles just befors glomerular capllaries

renine hypertension

renine hypotension RFhypertension.. ..hyperhypoB Excretory functions :

endogenous toxins..toxins.. : failuretoxic effect appears so earlyacute & chronic& includeurea , acetotic materials ( organic acid ) , K+ , phosphorus & uric acid failureacute RF chronic

- & include urochrome pigment, phenolic materails , aluminium

-RF- urea = Azot so, uremia = azotemia )main site of excretion)kidney)urea .. ):) through saliva :

salivation


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)bad taste of any thing(..urea(..) ..destructiontaste buds.... uremic smell or amonia smell

2 ) through GIT secretions - stomach irritationgastric mucosagastritisheart burn

(..) ..hematemesis..gastric ulcergastritisgastritis..vomiting (..melena(black stool

- colon secretions leading to colitis

NB. Colon contain stretch receptors soinal..colon wall..stimulation..spinal reflexstoolstool..contractionstoolsegment rectum & anus

(defecation reflex)irritation()stretch receptors..motility of colon..desire todef..(ulcer.. )dysentry.

( not amoebic dysentry .. not bacillary ( shigella ) dysentry .. but uremic dysentry )3 ) through sweat : ....irritation

to H1(receptors of histamine)itching effect .... ..-..

called urea frost()4 ) through Resp. secretions

ureasecretions of bronchus..airway..chestairway..(cough) (chest..chest free ((.. bleedinghemoptysisulceration..


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chestbronchospasm..(wheezing.. ) asthma(wheezeasthma) kidney(manifestations )....

- suppression to cyclooxygenase Enz. Inside the platlet ( ) leading to thrombathenia RFthrombocytopenia..purpuraRF.. .2- deposition on cell membrane of RBCs rupture hemolysis ( due to deformity of cell membrane )

3- suppression to lipase enz. cholesterol hypercholestremia in RF

liver Fhypochole. post. Strept. GNexcess fatRF4- if urea reach brain leading to

- irritation of vomiting center ( chemoreceptor triger zone )

F-A local cause gastritis B central cause irritation of vomiting center

- to arousal center ( reticular formation )

comadrousy manifestations of azotemia.... ..serosal membranes- pericardium dry pericarditis

2- pleura dry pleursy

3- peritoneum dry peritonitis

1,2 & 3 all leading to stitching pain

2- organic Acid :

kidney- PH..organic acids(PHalkalineacidic..) organic acidsactive process..reabsorptionbicarbonatePH acidosis


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...kidneyacidosis:

- failure of excretion of organic acid

- loss of bicarb. In urine

acidosis-- Kussmaul respiration ( air hunger ) : WHY ?? PHresp. system..organic acidslung..CO2 + H2O

CO2irritaterespi.centerleading to deep respiration..Kussmaul respiration ( air hunger ) CO2..Acidosis

so, air hunger is a compensation for acidosis .

2- rickets if still growing bone( due to melting of bone ) bicarbbonebicarb..boneCa-carbonate..Ca boneRickets

- so, Rickets has 2 causes in RF :

- failure of activation of vit D

- Ca from as a compensation to bicarb level ( )3- K+ in RF K+ level

normal level 3.5 5

- manifestations of K+ level :- irritation of SA node SA node tachycardia .

- motility of GIT K+motility motilitycolic..diarrhea(absorption)-:

- urea colitis dysentry

- K+ motility of GIT

NB . effect of K+ on skeletal Ms is the opposite of of its effect on smooth Ms ..skeletal MshypotoniatoneK+4- Phosphate :

- RF no excretion of Ph WHY ??

PhCa..parathyroid hormoneParathormone leding to excretion of Ph & reabsorption of Ca


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Ca..( ..parathormonereceptors)kidneyP

so, in urine Ca & Ph ( )parathyroid glandCaPh......

:..parathyroid hormone- kidney - Bone ..osteoblast & osteoclast

parathormoneactivityosteoclast..bonePh & Ca(osteoblast( glandparathyroidparathormone..Ph kidney..PhCa & Ph..parathormone CaPh

Ph..PhCa....kidney parathormone..Viscous circle...parathormone Ri..X raycystsCa & Ph.. ostietis fibrosa cysticademinerlaized area(not cyst)

-RicketsRF..3:1- Vit D activation 2- acidosis leading to melting of bone 3- parathormone

5- Uric acid

-arthritis Microtoxins :- Phenolic materials : ( ..( RF..irritationAHCsfasciculation() (spontinous contraction of diaphragmHiccup(irritationphrenic n..

RF(hiccup occur in 30 % of RF)2- melanine degradation urochrome pigments urine

......pigment.. ...... ....(learurine)

pigment


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3- Alumonium ()() delivery..(pure.. -kidney.. RF..:

- frontal lobe affection memory disturbance

2- deposites in BM may pancytopenia

-thrombocytopeniaRF:a- thrombopiotein b- alumonium toxicity

- causes of purpura in RF :

1- causes of thrombocytopenia 2- urea thrombathenia

65endocrine & exocrine functions of the kidney..

functionkidney

C - Power of concentration & dilution : specific gravity()- specific gravity of urine normally = 1015 10301025

10301015..-specific gravityurine or plasma

specific gravityosmolarity.... Na- normal specific gravity of plasma = 1010 plasma(glomerular filtrate.. pecific gravityplasma protein( ..plasma protein specific gravityglomerular filtrateplasma

Gl. Filtrateproximal convoluted tubulereabsorptionNa & water..PC..specific gravity.. ..

So, specific gravity at loop of henle = 1010 reabsorption of water..reabsorption of Naloop of henle filteratespecific gravity1010 distal convoluted tubulesdependant on aldosterone..reabsortion of Na pecific gravity ..


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ollecting tubules..(gates.. )controled by ADH....nterstatialmereabsorption of water only ( not salt )

urinespecific gravity..specific gravity-= concentration of urine

-ADH....urine output + specific gravity BUT if ADH urine output + specific gravity

(kidney(& dilutionpower of concentration of urine- ..8-12.. (water intake) water intake....ADH.. : (+specific gravity..1030( (2.. )water intakeADH to basal level urine output + specific gravity ( 1015 )specific gravitynormal1030 1015..( 1015.. )(1030)this is called normal power of concentration & dilution ( )

-:specific gravity ..() ...... .. ( ..(.. ()

- : during fasting..reabsorption of waterkidneyreabsorption of wover hydration. ..

- iterstatial medulla ( due to high osmolarity in it ) 2- ADH


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-RFinterstitial medulla....ADH

glomerular filt..with specific gravity 1010 as plasma ( in acute & chronic RF ) (low specific gravity)

specific gravity..urine volumeglomerular filterate...... fixed

so, in RF urine has Low fixed specific gravity

Chronic RFDefinition :

- inability of the kidney to maintain body homeostatsis ( )Causes :

- in child < 5 years : renal anomalies..5Ch. RF- Hypogenesis , agenesis ( aplasia of the kidney ) or urinary tract anomalies

acutechronic- or any obstructive uropathy ( )

2- If child > 5 years

as polycystic kidney & alport's $

as GN or hemolytic iremic $

clinical manifestations :

- manifestations of azotemia( urea ) - saliva as bad taste ..etc

- bad odour of mouth

- stomach d- colon e- sweat f- bronchial secretions

- chest pain or abdominal pain h- CNS affection

-34(..)

2- Air hunger ( rapid deep resp. ) due to acidosis ( metabolic ) due to :a- loss of HCO3 in urine b- failure to excrete acidic materials

3- urine volume : kidney(2)glomerular filterate24180=180 000 ml / 24 hrs urine output = 500 1500 ml / m2 / 24 hrs


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400oliguria..180anuria..1500polyuria urine (if nephrons < 0.5 milion(renal impairment (..:(2 000 000 nephrons give 180 000 ml

So, 200 nephrons give 18 ml & 100 nephrons give 9 ml 100 000..0.5chronic RF ..As 100 9 so , 100 000 give 9000 ml ....polyuria9urine volume.. ....2-3..10 000

10 000 900 ml urine output .. ..1000

So, 1000 90 ml ( oliguria even anuria according to surface area )

hronic RF rine volume -Polyuria normal oliguria or anuria or even absolute anuria

complications : ( ) - Racketic manifestations = renal osteodystrophy ..- no hydroxylation of vit. D in kidney

- acidosis melting of bone Ca

- Ph parathotmone osteitits fibrosa cystica

2- pallor or manifestations of anemia : WHY ??

- production of RBCs due to :

- erythropiotein

2- BM suppression by alumonium toxicity

3- iron & folic acid as a requirements ( ) iron & folic acid..

ammonia..iron & folic acid.- loss :

- hemolysis of RBCs by urea & other toxins .


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2- He due to bleeding tendancy

3- bleeding tendancy :

- thrombocytopenia - thrombathenia- Coagulopathies as urea prevent activation of coagulation factors

4- Growth failure ( dwarfism short stature ) - renal osteodystrophy HOW ??

-deformitybone - restriction of protein in diet .

- anemia ( chronic )

d- uremia suppress GH receptors leading to end organ resistance to GH .

5- CVS complications :

A- Hypertension WHY ??

- renin ( if irritative pathology ) Na & water retention .

2- End stage renal failure volume overload ( )3- cholesterol ( hyperlipedemia )

B Pericarditis

C HF WHY ??

- hypertension

2- end stage RF hypervolemia

3- anemic HF

4- toxic mycarditis ( due to uremia or other toxins )

6- Neuropsychatric disorders : due to :

- urea

- hypertensive encephalopathy

- trace elements & vitamins d- Aluminium toxicity

7- recurrent infections due to suppression of immune system by uremic toxins .

Investigations :


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- urine analysis : Low fixed specific gravity ( 1010 )

volume 2- urea & creatinine elevated .

3- CBC

normocytic normochromic

or microcytic hypochromic (iron )

or macrocytic normochromic (folic acid )

4- Bl. Gases metabolic acidosis

5- Electrolytes :

Na if renin ( irritative pathology ) & Na if renin ( destructive pathology )

K+ excretionactive process..Ca ++ decreased - Ph increased

alkaline phosphatase as he has RICKETS .

6- ECHO 7- assessment of nutritional state

Level of serum albumin , transferring , zinc , iron , folic acid , lipid ..etc

8- assess tone

9- investigations to detect etiology ....(heridatry)

ttt :

- Diet ( ) hronic RF- CHO

-....- Fat give digested fat

-medium chain triglyceridesfat....1 gm9.. renal transplant


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- protein ...uread- minerals

or is there salt loss or retention ??

(skimmed milk.. )fat .... ...... Ph excretion..as Posphate binder

- vitamins

increase fat soluble Vit. increase water soluble vit . ( )

dialysis..water soluble vit..f- water :

- if oligurai or anuria give urine volume + 400 ml / m2 / day ( fliud chart )

2- ttt of complications :

hypertension

anemia by dialysis ( aluminium ) + give iron & folic acid + erythropiotein

Rickets :

give active vit D

correct acidosis

if resistant cases parathyroidectomy

3- dialysis : ??if GFR = 10 ml / minute

or severe manifestations of azotemia

or K+ reach 7 tachyarrythmia-..manifestations..dialysis

4- Renal transplantation 5- social & psychological ttt 6- Drug dosage


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kidney..- 76Acute renal failure

written Definition acute renal failure kidneystop of filteration: .waste products ARF may be reversible..chronic urine outputfilteration.. ..oliguria..chronic-..ARF

Causes : : filteration..filteration filteration- glomerular capillary pressure (plasma protein) (afferent)diameter..efferent().

Afferent diameter : efferent diameter = 7 : 1

capillary pressure.2- Bowman's capsule

-filteratepressure.3- basement membrane & the whole nephron :

))ARFARF..-

glomerular capillary pressure : ( called prerenal causes ) - Dehydration ( Blood volume )

-dehydration:- loss of fliud ( as in diarrhea , vomiting , polyuria , excessive sweating )

- intake of fluid as in fasting dehydrationDehydration Blood volume renal blood flow ( RBF ) glomerular capillary pressure

filteration that may leading to ARF according to severity of dehydration


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2- loss of blood as Hge same mechanism as dehydration .

3- shock as- hypovolemic shock or other tyoes of shock that leading to VD of peripheral bl vessels

renal arterial pressure..RBF........................etc4- post surgery cardiac surgery ..motilityintestine.. paralytic ileus IV fluids..motility

.. (passingoral intake Flatus.... )not stool.. (!!) ....auscultationmotility.dehydration..IV fluids ....renal functionsureacreatinie renal impairment ....mo

5- Nephrotic $ : urine..osmotic pressure..vesselsintrerstasevere cases..blood volume.......... interstatiumintravascular

-pre renal causesthere is Hypotnsion

Bowman's capsule pressure ( called post renal causes ) obstructionpathwayurine..:- Acquired :

- as stricture pf urethra or stone .

2- congenital :

- posterior urethral valve fold of mucosaurinationurethraobstruction- obstruction..retention of urinebladder..back pressureureter

pelvis of kidn

then back pressure to all nephron's parts then to Bowman's capsule

filteration..blood volumeso, hypervolemia & hypertension


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2back pressure( ..)urethraobstruction..ki

kidney( ..ureter..unilateral obstruction( renal impairment..single..unilateral obstructionARF

functioning k

Renal causes as :- filter closure( ) acute GN..nephritic..

odema or proliferation of cells of BM.. ..2- nephrons destruction ( ) as in severe anoxic tubular necrosis (dehydration(diarrhea ..

renal ischemia..nephrons..pre renal cause .3- toxins as all nephrotoxic drugs as

all anesthetic drugs

aminglycosides gastroenteritisdehydrated..aminoglycosidesprerenal cause

carbon tetrachloride

4- infarction as an effect of embolus 5- congenital anomalies :

- agenesis ( ) or hypogenesis-renal..bl. Volume..Hypertension

pre , post or renal..ARF pre renal ..do catheterization..post or renalbladder..renal ()urinepost renal

Clinical picture :-acute renal failure..macrotoxins

- oliguria or anuria


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..-magor toxins:

2- urea manifestations of azotemia 3- metabolic acidosis manifestations as air hunger acute RFretention of organic acid..loss of bicarb..acidosis

filteration( chronic.4- manifestations of hyperkalemia as :

tachycardia due to stimulation os SA node .

abdominal colic & diarrhea ( motility of intestine )

generalized ms. Weakness & hypotonia

NB. NO manifestations of hyperphosphatemia or hyperuricemia

chronicInvestigations :- urine analysis

2- 3 cm urine(24)- volume oliguria ( < 400 ml / m2 / 24 hrs )- low fixed specific gravity ( 1010 )

-urine..specific gravity.. specific gravityARF end stage chronic renal failure..- RBCs casts

-RBCsmucoproteind- Na 2- serum analysis : urea & creatinine - K & uric acid ( all major toxins increased )

Na dilutional hyponatremia-post & renalpredehydration 200 ml water..container. .. 130 mEq / L

NB. mEq = milliequivalents


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....600 ml water+2container ..(300 %..10) post renal & renal..filteration..salt & water

rete..Naretainedsalt..dilutionalhyponat

3- ECG (..) 4- investigation of underlying etiology .

Treatment : acute......hronicRF

-:- history of precipitating factors .

- oliguric

- rapid deep respiration LINES OF ttt

- measure Bl. Pressure if low : pre renal..low.....glomrular capillary pressu....ringer lactate acidosisbicarbonate..liverlactate

dose20 ml / Kg( emergency)..(bl. Volume) ..filteration..urine.. ..mannitolosmotic diuresis..urine . lasix.. chronic....urine..

RF(nephronsanoxic tubular necrosis)2- If High Bl. Pressure : so, renal or post renal ..post renal.... renal functions..obstruction.3- if renal : renalfilterationurine..


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post. Streptococcal GN(fliud chartK complicationsdialysis) ..lasix..pre renallasix:-

Urinary Hueswrittenurine-

A - Dark urine : :- retained urine :

-retained urine..urochrome pigment- bile pigments

-obstructive Jdirect bilirubin...B red urine :

red urine-- hematuria

2- hemoglobinuria 3- myoglobin in urine

ms....- myoglobin(Hb)4- porphyrin

-Hbiron + protoporhyrin5- Iron in chronic hemolytic anemia ..chelating agents ....desferroxasmineiron urine6- urates 7- Drugs rifampicin ( rimactan )8- Foods as beets .... ()C Dark brown or black urine :


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- melanine deposites as in melanoma

2- homogentisic acid -tyrosine:

Tyrosin give para hydroxy phenyl pyruvate by tyrocinase .

then para hydroxy phenyl pyruvate give homogentisic acid by para hydroxy phenyl pyruvate oxidase .

then homogentisic acid give succinic acid by homogentisic acid oxidase .

then succinic acid excreted in urine . homogentisic acid oxidase..homogentisic acidurine ..sclera..cartilage lkaptonuriaHematuria

RBCsurine> 5 RBCs / high power field of microscope ( HPF ) ..urineRBCs..Types

2 types

- Microscopic .. 2- Macroscopic

CausesA Glomerular causes :

ALL CAUSES OF NEPHRITIC-:

- Alport's , IgA nephropathy , SLE , anaphylactoid purpura , Post streptococcal GN , proliferative GN

progressive GN etc

B Non glomerular causes urethrapelvis od the kidneyurinary tract- Congenital anomalies as :

- polycystic kidney

hematuria..cyst-- hemangioma in kidney pelvis leakage hematuria .

2- Infections in urinary tract :

- acute pyelonephritis or cystitis

-infections../UTI.3- Tumors as wilms tumor


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hematuria..ery late(advanced) hypernphroma..ematuria(arly wilmscortex..medulla(hematuria)hypernephromamedulla

4- Drugs: as cyclophsphamide that cause Hemorrhagic cystitis .

5- Vascular cause :

as renal infarction , renal vein thrombosis , leading to congestion of the kidneyhematuria6- trauma :

extrenal trauma internal trauma as stones

))C I N D V T( .. )C

I

N

D

V

T

7- exercise induced hematuria : -heavy exercise..hematuria

- erect position congestion of kidney exercise- during exercise may minir trauma

DD between glomerular & non glomerular causes : glomerula...

non.. ..relation to micturation....glomerula...

non: urinary bladder urethra


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Nephrology Prof. Dr. Abo El-Asrar oligurai , odema & hypertension

glomerula..nephriticnon.. : urethra..

bladder..suprapubic refion pyelonephritis..loin pain(..) ........... urine analysis

glomerular casts , protein >= +2

if non glomerular no casts , proteinuria < +2

.. +..nephrostomy pelvis of the kidney..ureter..:

() 20 17

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Nephrology - Dr Abo-ElAsrar - By El Azhar Medical Students 2012

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